Acrochordons as a cutaneous sign of impaired carbohydrate metabolism, hyperlipidemia, liver enzyme abnormalities and hypertension: A case-control study.

BACKGROUND: Acrochordons are common and benign skin tumours. A few studies with contradictory results have been reported regarding the abnormalities of carbohydrate and/or lipid metabolisms in patients with acrochordons. OBJECTIVES: We aimed to determine if the presence of acrochordons could be a marker of diabetes, hyperlipidemia, liver enzyme abnormalities and hypertension by comparing with a control group. METHODS: A total of 110 patients having two or more acrochordons and age- and gender-matched 110 controls were included in the study. Localization, size and the total number of acrochordons were recorded in the patient group. Fasting plasma glucose (FPG), serum lipids and liver enzyme levels were tested in patient and controls. All participants underwent a standard 2-h oral glucose tolerance test with 75 g glucose. Diabetes mellitus and impaired glucose intolerance were diagnosed according to the American Diabetes Association criteria. Arterial blood pressures were measured in two groups. RESULTS: A total of 56 patients and 10 controls were diagnosed with overt DM. Thirteen per cent of the patients and 9% of controls had an impaired glucose tolerance test. The difference was statistically significant for the diagnosis of DM and not significant for the impaired glucose tolerance. The mean levels of FPG, total cholesterol, LDL cholesterol, triglyceride, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase and alkaline phosphatase were significantly higher in patients than those in controls. Furthermore, serum levels of HDL were less in patients. Patients with acrochordons had higher systolic and diastolic blood pressures than controls. CONCLUSIONS: The results of our study suggest that acrochordons may represent a cutaneous sign for impaired carbohydrate or lipid metabolism, liver enzyme abnormalities and hypertension.

Prevalence of the DNA repair enzyme-NEIL1 gene mutation in patients with type 2 diabetes in the Turkish population.

In spite of the fact that an indirect relationship between NEIL1 gene and Type 2 diabetes has been demonstrated in animal model studies, there have been no human studies showing this relationship. In our study, we aimed to show the relationship between NEIL1 mutation and Type 2 diabetes in humans. The study group consisted 70 patients with Type 2 diabetes and the control group consisted of 50 healthy individuals. The mean age was 53±11 yr and 49±11 yr, respectively. Two NEIL1 mutations (2.9%) were detected in the patient group. There was A→G change (133A→G) at the 133. position of the 8th exon with 257 bp length in base sequencing. There was no mutation in the control group. We searched NEIL1 gene mutation for the first time in patients with Type 2 diabetes. This mutation was "silent" as it did not cause any amino acid change. The effects of these mutations on the etiopathogenesis of disease are not known. Although the lysine encoded by AAG was identical to the lysine encoded by AAA, it is not clear if they have functional differences due to the changing environmental conditions. NEIL1 gene mutation may have causative role in the development of Type 2 diabetes.

Acrochordons as a cutaneous sign of impaired carbohydrate metabolism, hyperlipidemia, liver enzyme abnormalities and hypertension: a case-control study.

Background Acrochordons are common and benign skin tumours. A few studies with contradictory results have been reported regarding the abnormalities of carbohydrate and/or lipid metabolisms in patients with acrochordons. Objectives We aimed to determine if the presence of acrochordons could be a marker of diabetes, hyperlipidemia, liver enzyme abnormalities and hypertension by comparing with a control group. Methods A total of 110 patients having two or more acrochordons and age- and gender-matched 110 controls were included in the study. Localization, size and the total number of acrochordons were recorded in the patient group. Fasting plasma glucose (FPG), serum lipids and liver enzyme levels were tested in patient and controls. All participants underwent a standard 2-h oral glucose tolerance test with 75 g glucose. Diabetes mellitus and impaired glucose intolerance were diagnosed according to the American Diabetes Association criteria. Arterial blood pressures were measured in two groups. Results A total of 56 patients and 10 controls were diagnosed with overt DM. Thirteen per cent of the patients and 9% of controls had an impaired glucose tolerance test. The difference was statistically significant for the diagnosis of DM and not significant for the impaired glucose tolerance. The mean levels of FPG, total cholesterol, LDL cholesterol, triglyceride, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase and alkaline phosphatase were significantly higher in patients than those in controls. Furthermore, serum levels of HDL were less in patients. Patients with acrochordons had higher systolic and diastolic blood pressures than controls. Conclusions The results of our study suggest that acrochordons may represent a cutaneous sign for impaired carbohydrate or lipid metabolism, liver enzyme abnormalities and hypertension.

The significance of coeliac disease antibodies in patients with ankylosing spondylitis: a case-controlled study.

The presence of anti-gliadin antibodies (AGA) and their relationship with intestinal permeability and prevalence of undiagnosed coeliac disease (CD) in ankylosing spondylitis (AS) were investigated. Blood samples from 30 AS patients and 19 age- and sex-matched controls were analysed for human leucocyte antigen (HLA)-B27, AGA and endomysial antibodies (EMA). Immunoglobulin (Ig) A-type AGA and IgG-type EMA were determined by enzyme-linked immunosorbent assay. AGA-positive patients were examined by gastroduodenoscope and proximal small bowel mucosa biopsies were performed. Eleven (36.7%) AS patients were AGA positive (compared with none of the control subjects) and three (10.0%) of these AS patients were also EMA-positive. The presence of AGA was not associated with more severe AS. Mild-to-severe villous atrophy and hyperplasia of crypts with increased chronic inflammatory cells in the lamina propria, which is typical of CD, was only observed in one AGA/EMA positive AS patient; CD was subsequently diagnosed by histology. Although AGA positivity might contribute to the pathogenesis of AS by increasing intestinal permeability to micro-organisms or by modifying intestinal immune mechanisms, further work is required to clarify its role in AS.

Does rofecoxib increase TNF-alpha levels?

OBJECTIVE: Rofecoxib (Vioxx), the first COX-2 selective non-steroidal anti-inflammatory drug (NSAID), was recently withdrawn from the market due to the increased risk of acute myocardial infarction. The precise mechanism responsible for this phenomenon still remains unknown. Tumor necrosis factor alpha (TNF-alpha) is a cytokine, possibly most responsible for mortality in patients with acute myocardial infarction. However, this study was designed to study possible effects of rofecoxib on the level of TNF-alpha by using MSU crystal induced inflammation in the rat subcutaneous air pouch model. METHODS: Rat subcutaneous air pouches were produced and examinations commenced 6 days later. Control groups received only MSU crystals, or no crystals or drugs. To begin with, rofecoxib (30 mg/kg), indomethacin (20 mg/kg) or diclofenac (3 mg/kg) were administered to groups of 5 rats each. Thirty minutes later, MSU crystals were injected into air pouches, except for the negative control group. Twenty-four hours later, the rats were sacrificed for aspiration of fluid and for the dissection of pouch walls to determine leukocyte counts, pouch wall histology, and to assay IL-10 and TNF-alpha. RESULTS: Intra-pouch injection of MSU crystals, compared to non-injected pouches, caused an increase in white blood cell count (WBC) (30 +/- 44.7 versus 4508 +/- 792.3 cells/mm3), in the numbers of pouch wall vessels (vascular index) (4.8 +/- 0.3 versus 11.4 +/- 1.5 vessels/high-power field) and in TNF-alpha (50.0 +/- 13.4 versus 70.34 +/- 20.9 ng/mL), but not in interleukin-10 (IL-10) (60.6 +/- 63.0versus 61.48 +/- 7.1). WBC and vascular index were significantly reduced in all study groups compared to the control group (p < 0.05). Levels of TNF- in fluids were unexpectedly and significantly (p < 0.05) increased in all cases. The highest level of TNF-alpha was found in the rofecoxib group. In contrast to TNF-alpha, IL-10 levels were significantly (p < 0.05) decreased in all three drug groups. Indomethacin tended to suppress inflammation more effectively. However, there was no significant difference between the groups for IL-10 (p > 0.05). CONCLUSION: All three NSAIDs exhibited anti-inflammatory activity against MSU crystal induced inflammation. The difference in anti-inflammatory effects of these three non-steroidal drugs is seen not only in the anti-inflammatory effect on MSU induced inflammation but also in the nature of the effects. Refocoxib tended to increase the TNF-alpha level. Whether increased TNF-alpha levels can help explain the side effect of COX-2 specific inhibitors still requires further studies.

Hemostatic changes in active pulmonary tuberculosis.

OBJECTIVE: Severe pulmonary tuberculosis (PTB) is sometimes complicated by deep vein thrombosis (DVT). We have searched for possible hemostatic disturbances that are predisposing factors for venous thrombosis in patients with PTB. DESIGN: Coagulation and platelet function tests were studied in 45 patients with active PTB and 20 healthy control volunteers before therapy. Findings were compared with results at 30 days. RESULTS: Analysis in patients with active PTB showed anemia, leucocytosis, thrombocytosis, elevation in plasma fibrinogen, factor VIII, plasminogen activator inhibitor 1 (PAI-1) with depressed antithrombin III (AT III) and protein C (PC) levels. On the 30th day of treatment, anemia, leucocytosis and thrombocytosis were improved. Fibrinogen and factor VIII levels had decreased to normal levels, PC and AT III levels had increased to normal levels, and there was no difference in PAI-1 levels. We found no activated protein C resistance. Platelet aggregation studies demonstrated increased platelet activation. However, DVT was not detected in patients during the follow-up period. CONCLUSION: Decreased AT III, PC and elevated plasma fibrinogen levels and increased platelet aggregation appear to induce a hypercoagulable state seen in PTB and improve with treatment.

CagA status in dyspeptic patients with and without peptic ulcer disease in Turkey: association with histopathologic findings.

BACKGROUND: CagA seropositivity is closely associated with that of vacuolating cytotoxin (VacA). Helicobacter pylori strains positive for both VacA and CagA were reported to be strongly associated with peptic ulcer disease. Different results reporting that cagA gene is not associated with more serious diseases, lowers the importance of CagA protein as a marker. In this study, CagA seropositivity is examined in Turkish peptic ulcer and nonulcer dyspepsia patients; histopathologic scores of CagA (+) and CagA (-) groups were compared. MATERIALS AND METHODS: Sixty consecutive patients (one gastric ulcer, 13 duodenal ulcer and 46 nonulcer dyspepsia) (mean age 40.9 +/- 14.7; 33 women, 27 men) with dyspeptic complaints who underwent upper gastrointestinal (GI) endoscopy were included. Biopsies from the antrum and corpus were used for histopathologic examination and for rapid urease test. H. pylori-negative patients comprised the control group. Histopathologic findings were graded using a previously described grading system (for inflammation, activity, atrophy, intestinal metaplasia and H. pylori, grades from 0 to 3 were used to quantify the findings). In H. pylori-positive patients, antibodies against CagA protein were determined using an ELISA METHOD: RESULTS: H. pylori was (+) in 46 patients. One duodenal ulcer and 13 nonulcer dyspepsia patients were negative for H. pylori. CagA positivity is significantly higher in peptic ulcer patients [12/12] than in nonulcer dyspepsia patients [25/33]. While inflammation, activity and atrophy scores were significantly higher in CagA positive patients, intestinal metaplasia and H. pylori load scores were not. Although the histopathologic scores in controls were lower than CagA (-) group, statistical significance was observed only in inflammation and intestinal metaplasia scores. CONCLUSION: Development of more prominent gastritis and severe atrophy in CagA (+) patients is an indicator of the importance of CagA rather than H. pylori load. Therefore, we suggest that nonulcer dyspepsia patients should also be tested for CagA status along with the tests for H. pylori status; and a positive CagA testing should be considered as an indication for eradication treatment. If CagA is negative, further assesment should be performed to decide whether or not to treat the patient.